Enveloped animal viruses attach to and enter the host cell via the interaction of viral proteins in the virion membrane (envelope proteins) and cell surface proteins (virus receptors). Receptor recognition and binding are mediated by the surface envelope protein. Virus entry is an attractive target for anti-viral treatment; numerous entry inhibitor drugs that are designed to block HIV receptor (CD4) attachment, co-receptor (CCR5, CXCR4) engagement, or host cell-virus membrane fusion have been or are currently being evaluated in preclinical or clinical studies (Richman, 1998; PhRMA, 1999; Stephenson, 1999). For example, the co-receptor antagonist vicriviroc (SCH-D, Schering Plough), which blocks the interaction between the viral membrane surface protein (gp120) and CCR5, is currently being evaluated in clinical studies for its effectiveness as an anti-viral treatment (Shurman, 2004). Other entry inhibitors currently or previously under investigation include UK-427857 (maraviroc, Pfizer), TNX-355 (Tanox Inc.), AMD-11070 (AnorMED), Pro 140 and Pro 584 (Progenies), FP-21399 (EMD Lexigen), BMS-488043 (Bristol-Myers Squibb), INCB9471 (Incyte), KRH-3955 and KRH-314 (Kureha), HGSImAb004 (Human Genome Sciences), TRI-999, (Trimeris) and GSK-873,140 (aplaviroc, GlaxoSmithKline). One entry inhibitor, FUZEON® (enfuvirtide; Roche/Trimeris), has been approved for treatment of HIV infection by the United States Food and Drug Administration.
As these drugs continue to be developed and enter the clinic, assays are needed that can rapidly and easily identify patient populations that may clinically benefit from administration of these drugs. These and other unmet needs are provided by the present invention.